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强直性脊柱炎中广泛椎体破坏的发病机制。

The pathogenesis of extensive discovertebral destruction in ankylosing spondylitis.

作者信息

Wu P C, Fang D, Ho E K, Leong J C

机构信息

Department of Pathology, University of Hong Kong.

出版信息

Clin Orthop Relat Res. 1988 May(230):154-61.

PMID:3365888
Abstract

The study of extensive discovertebral destructive lesions in ankylosing spondylitis has been largely limited to isolated case reports or clinicoroentgenologic reviews with little pathologic correlation. In eight specimens of the spine collected from 35 patients with ankylosing spondylitis showing extensive discovetebral destructive lesions, a detailed pathologic study revealed a consistent picture of complete or near-complete destruction of the disc-bone border and the intervertebral disc. The disc was replaced by fibrous tissue and/or fibrocartilage showing moderate to severe fibrinoid necrosis and cystic degeneration. Such changes are characteristic of pseudarthrosis, which may follow either fracture or degeneration of the disc perpetuated by abnormal stress and motion. The reparative process included fibrovascular tissue proliferation from the vertebral bone marrow. Fibrovascular tissue also perforated the vertebral end-plate and intervertebral spaces resulting in massive discovertebral destruction. Pathologic observations strongly implicate mechanical trauma and pseudarthrosis as initiating and perpetuating extensive discovertebral destruction in ankylosing spondylitis.

摘要

对强直性脊柱炎广泛的椎间盘破坏性病变的研究,很大程度上局限于孤立的病例报告或临床放射学综述,病理相关性很小。在从35例患有广泛椎间盘破坏性病变的强直性脊柱炎患者中收集的8个脊柱标本中,详细的病理研究揭示了椎间盘-骨边界和椎间盘完全或近乎完全破坏的一致情况。椎间盘被纤维组织和/或纤维软骨取代,表现出中度至重度的纤维素样坏死和囊性变。这些变化是假关节的特征,假关节可能继发于因异常应力和运动而持续存在的椎间盘骨折或退变。修复过程包括来自椎骨髓的纤维血管组织增生。纤维血管组织还穿透椎体终板和椎间隙,导致广泛的椎间盘破坏。病理观察强烈提示机械性创伤和假关节是强直性脊柱炎中广泛椎间盘破坏的起始和持续因素。

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